Re: symposium # 723
Dr. Anton Lukas
On Tue Dec 8, Adel Elmoselhi wrote
>Hi Dr. Lukas, very interesting study. I was just wonder if it is known which isoform of PKC is activated for each G-protein receptors. Since you have shown kind of an opposite functions for different PKC isoforms, with PKC-delta and PKC-mu protect cell injury and decrease arrythmogenesis, while PKC-zeta induces contractile dysfunction during ischemia, so what would be the net result especially in a tissue that has different isoforms, does it depends on their expression or the receptors that activate them or something else. It would be really interesting to understand the mechanism(s).
You have raised an interesting point. At present, little is known about the coupling of specific G-protein receptors to PKC isoforms in the heart. There is evidence to suggest that adenosine A1 receptors couple to PKC through PLC and adenosine A3 receptors couple through PLD. However, it is not known which isoforms of PKC are coupled to specific receptors and whether they vary with species (i.e., rat versus rabbit). Clearly, a lot more work is required to elucidate the coupling of G-protein receptors (such as adenosine, alpha1-adrenergic, bradykinin, angiotensin II, etc) to specific PKC isoforms.
Tue Dec 8